icn victoria: john botha on critical care renal failure

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Professor John Botha from Frankston Hospital in Melbourne talks at the April 2014 Victorian Intensive Care Network meeting on Renal Failure in Critical Care

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  • PENINSULA HEALTH c12 classification by the College of Intensive Care Medicine The Problem with Acute Renal Failure John Botha MBChB M Med FCP(SA)FRACP FCICM Dip PG Echo Dip Neph Director of Intensive Care Peninsula Health Adjunct Clinical Professor Monash University Peninsula Health, Winner Metropolitan Health Service of the Year 2007 and 2009 2
  • Why is Hospital Acquired AKI a problem for the bedside clinician? Renal Physiology is Complex Markers of Renal Injury are not clinically used(or useful?) Fluid management in Sepsis is Difficult and overzealous administration is bad The role of the endothelial glycocalyx in fluid distribution is important and its integrity is difficult to measure Fluid Types may impact on Renal Outcome Therapies for AKI with RIFLE Risk and Injury are limited High Intensity RRT has not proven benefit Optimising Filter life is problematic In patients who have RRT in ICU the outcomes is poor
  • Problematic physiology 1. The kidney is at risk of hyperoxia 2. The kidney is at risk of hypoxia
  • The kidney has a high exposure to O2 Oxygen tension is tightly regulated in all organs because high PO2 is toxic In the kidney superoxide production is tightly dependent on O2 availability
  • The human kidney has structural antioxidant defences. Arteries and veins are closely associated This facilitates counter-current diffusion and enables a high degree of AV shunting
  • Renal veins have a unique peri-arterial structure It facilitates diffusive O2 shunting
  • Close coupling of veins and arteries to achieve counter-current O2 diffusion
  • This shunting is dependent on Renal Blood Flow
  • The cortex and the medulla Are linked by shunting If the cortex is underperfused More AV shunting occurs in interlobular vessels This can lead to medullary ischemia Even if medullary flow is preserved
  • Medullary PO2 is very low
  • The septic kidney: global renal blood flow
  • Intra-renal blood flow In septic sheep
  • Intra-renal oxygenation Cortico-medullary dissociation Knowing global Or even intra-renal blood flow says little about medullary oxygenation
  • Clinical implications Global renal blood flow may be dissociated from GFR, medullary flow and medullary O2 Reliable ways to measure renal blood flow are not available If there were reliable therapies to increase renal blood flow the effect of this on GFR is unpredictable. The renal medulla is always at risk of hypoxia
  • Biomarkers for the prediction of acute kidney injury: a narrative review on current status and future challenges Hilde R. H. de Geus, Michiel G. Betjes and Jan Bakker Clin Kidney J (2012) 5 (2): 102-108 Biomarkers for AKI Functional markers- SCr and plasma/serum CyC Up-regulated proteins -NGAL, KIM-1, L-FABP and IL-18 Low-molecular weight proteins -Urine CyC Enzymes NAG,- a-GST, p-GST, GGT and AP Markers of Renal Injury are not clinically used(or useful?)
  • The reported AUCs are disappointing ranging from 0.50 to 0.84, with one or two exceptions, which can be explained by statistical or methodological differences in study design. The discriminatory function in heterogeneous populations is poor and influenced by pre-existing renal function and time of sample collection with respect to the renal insult Clinical appraisal of a patient using standard parameters such as SCr and diuresis remains the cornerstone for now Reasonable to use biomarkers together with other parameters such as traditional clinical characteristics to optimize the accuracy of prediction of developing AKI
  • Acute Renal Failure in the Critically Ill Multinational Multicentre Study JAMA August 17 2005 Vol 294 Septic Shock Major Surg Cardio Shock Hypo Vol Drug HRS Obstr Uro Other 47.5% 34.3% 26.9% 25.6% 19% 5.7% 2.6% 12.%
  • MORTALITY 0% 10% 20% 30% 40% 50% 60% ICU WARD
  • Fluid management in Sepsis is Difficult and overzealous administration is bad Fluid resuscitation in septic shock- A positive fluid balance and elevated central venous pressure are associated with increased mortality Boyd, John H. MD, FRCP(C); Forbes, Jason MD; Nakada, Taka- aki MD, PhD; Walley, Keith R. MD, FRCP(C); Russell, James A. MD, FRCP Critical Care medicine Feb 2011 Vol 32
  • Design VASST Study Patients: The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock A retrospective review of the use of intravenous fluids during the first 4 days of care.
  • Based on net fluid balance, they determined whether fluid balance quartile correlated with 28-day mortality
  • Table 1 Table 1. Fluid intake, urine output, and net fluid balance at 12 hrs and cumulative day 4 balance Copyright 2011 Critical Care Medicine. Published by Lippincott Williams & Wilkins. 31 Fluid resuscitation in septic shock: A positive fluid balance and elevated central venous pressure are associated with increased mortality* Boyd, John H.; Forbes, Jason; Nakada, Taka- aki; Walley, Keith R.; Russell, James A. Critical Care Medicine. 39(2):259-265, February 2011. doi: 10.1097/CCM.0b013e3181feeb15
  • Figure 2 Figure 2.A, Cox survival curves, adjusted for age, Acute Physiology and Chronic Health Evaluation (APACHE) II score, and severity of shock (dose of norepinephrine), are shown for fluid balance quartiles at 12 hrs. Quartiles 3 and 4 have significant increases in mortality compared with both quartiles 1 and 2 . B, Cox survival curves, adjusted for age, APACHE II score, and dose of norepinephrine, are shown for cumulative fluid balance quartiles at day 4. Quartiles 3 and 4 have significant increases in mortality compared with both quartiles 1 and 2. Copyright 2011 Critical Care Medicine. Published by Lippincott Williams & Wilkins. 32
  • Table 2 Table 2. Hazard ratio for death according to fluid balance quartiles Copyright 2011 Critical Care Medicine. Published by Lippincott Williams & Wilkins. 33 Fluid resuscitation in septic shock: A positive fluid balance and elevated central venous pressure are associated with increased mortality* Boyd, John H.; Forbes, Jason; Nakada, Taka- aki; Walley, Keith R.; Russell, James A. Critical Care Medicine. 39(2):259-265, February 2011. doi: 10.1097/CCM.0b013e3181feeb15
  • A more positive fluid balance both early in resuscitation and cumulatively over 4 days is associated with an increased risk of mortality in septic shock
  • Next Question. Whether fluid balance was predictive of central venous pressure ? Whether a guideline-recommended central venous pressure of 812 mm Hg yielded a mortality advantage?
  • Figure 3 B, Day 4 fluid balance during the preceding 24 hrs does not correlate with central venous pressure nor with the dose of norepinephrine. Copyright 2011 Critical Care Medicine. Published by Lippincott Williams & Wilkins. 36 Figure 3.A, Fluid balance on study enrolment (12 hrs) significantly correlates with central venous pressure and dose of norepinephrine, p < .001 in both cases.
  • Figure 4 . B, Cox survival curves, adjusted for age, APACHE II score, and dose of norepinephrine, are shown for CVP groups on day 4. There were no significant differences in mortality among groups. Cright 2011 Critical Care Medicine. Published by Lippincott Williams & Wilkins. 37 Figure 4.A, Cox survival curves, adjusted for age, Acute Physiology and Chronic Health Evaluation (APACHE) II score, and severity of shock (dose of norepinephrine), are shown for central venous pressure (CVP) groups at 12 hrs. Patients with a CVP of 12 mm Hg had the highest mortality
  • Central venous pressure correlated with fluid balance at 12 hrs. On days 14, there was no significant correlation. At 12 hrs, patients with a central venous pressure 12 mm Hg. There was no correlation between CVP and mortality at day 4
  • However, in patients whose central venous pressure was ChiSq Hazard RatioLabel FilterGroup Hep/Prot 1 0.70736 0.20429 11.9888 0.0005 2.029FilterGroup 0 The hazard ratio for a filter experiencing clotting in the heparin/protamine group (compared to citrate) was 2.03 (95% CI 1.34-3.02, p